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Your Position: > LILRA4

LILRA4

요약

Name:Leukocyte immunoglobulin-like receptor subfamily A member 4
Target Synonym:ILT7,CD85g,Immunoglobulin-like transcript 7,LILRA4,Leukocyte Immunoglobulin Like Receptor A4,Leukocyte Immunoglobulin-Like Receptor, Subfamily A (With TM Domain), Member 4,CD85 Antigen-Like Family Member G,Leucocyte Ig-Like Receptor A4,Leukocyte Immunoglobulin-Like Receptor, Subfamily A (Without TM Domain), Member 4,Leukocyte Immunoglobulin-Like Receptor Subfamily A Member 4,CD85g Antigen,ILT-7
Number of Launched Drugs:0
Number of Drugs in Clinical Trials:1
Lastest Research Phase:Phase 2 Clinical

제품 리스트 구매

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제품번호 제품 설명 구조 순도 특징
LI4-H52H5 Human Human LILRA4 / CD85g / ILT7 Protein, His Tag
LI4-H52H5-structure
LI4-H52H5-sds
LI4-H5243 Human Human LILRA4 / CD85g / ILT7 Protein, His Tag (MALS verified)
LI4-H5243-structure
LI4-H5243-sds

일부의 생물활성 데이터

LI4-H5243-ELISA
 LILRA4 ELISA

Immobilized Human LILRA4, His Tag (Cat. No. LI4-H5243) at 2 μg/mL (100 μL/well) can bind Monoclonal Anti-LILRA4 Antibody, Human IgG1 with a linear range of 0.001-0.008 μg/mL (QC tested).

LI4-H5243-MALS-HPLC
LILRA4 MALS images

The purity of Human LILRA4, His Tag (Cat. No. LI4-H5243) is more than 95% and the molecular weight of this protein is around 55-74 kDa verified by SEC-MALS.

Synonym Name

LILRA4,CD85g,ILT7,ILT-7

Background

Leukocyte immunoglobulin-like receptor subfamily A member 4 (LILRA4/ILT7/CD85g) is a marker of plasmacytoid dendritic cells (pDCs), which are reported to be a major source of the abnormally high levels of IFNα associated with autoimmune diseases. Targeting LILRA4 with therapeutic antibodies to promote killing of these IFNα-producing pDCs is being investigated as a novel approach to alleviating the symptoms of autoimmune diseases. LILRA4 is an immunoglobulin-like protein preferentially expressed on the surface of human plasmacytoid dendritic cells (pDCs). It interacts with bone marrow stromal cell antigen 2 to control the Toll-like receptor (TLR) driven response by pDCs to viral infection. It may also be involved in modulating pDC-tumour interactions. pDCs are a source of the excess IFNα which drives autoimmune disease symptoms.

Clinical and Translational Updates

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